Role of the Gut–Liver Axis in Liver Inflammation, Fibrosis, and Cancer: A Special Focus on the Gut Microbiota Relationship

Ohtani, Naoko; Kawada, Norifumi

doi:10.1002/hep4.1331

Cited by 138 publications

(125 citation statements)

References 126 publications

(161 reference statements)

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“…The most likely scenario is via the gut-liver axis. Many studies have shown that the bacteria and bacterial products can reach the liver through the portal vein and liver secretory products, such as bile acids, IgA, and antimicrobial molecules, can leave the liver into the intestines through the biliary tract 40,41 . It is thus likely that infectious virus exits the liver through the biliary tract into the intestine where it exits the body in the stool, explaining the high stool titers with little to no infectious virus in the intestine itself.…”

Section: Despite the Clear Hepatic Tropism Of Echoviruses Little Is mentioning

confidence: 99%

Human FcRn expression and Type I Interferon signaling control Echovirus 11 pathogenesis in mice

Wells

Grimes

Kim

et al. 2020

Preprint

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Neonatal echovirus infections are characterized by severe hepatitis and neurological complications that can be fatal. Here, we show that expression of the human homologue of the neonatal Fc receptor (hFcRn), the primary receptor for echoviruses, and ablation of type I interferon (IFN) signaling are key host determinants involved in echovirus pathogenesis. We show that expression of hFcRn alone is insufficient to confer susceptibility to echovirus infections in mice. However, expression of hFcRn in mice deficient in type I interferon (IFN) signaling, hFcRn-IFNAR−/−, recapitulate the echovirus pathogenesis observed in humans. Luminex-based multianalyte profiling from E11 infected hFcRn-IFNAR−/− mice revealed a robust systemic immune response to infection, including the induction of type I IFNs. Furthermore, similar to the severe hepatitis observed in humans, E11 infection in hFcRn-IFNAR−/− mice caused profound liver damage. Our findings define the host factors involved in echovirus pathogenesis and establish in vivo models that recapitulate echovirus disease.

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Section: Despite the Clear Hepatic Tropism Of Echoviruses Little Is mentioning

confidence: 99%

Human FcRn expression and Type I Interferon signaling control Echovirus 11 pathogenesis in mice

Wells

Grimes

Kim

et al. 2020

Preprint

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“…The liver is directly exposed to gut microbial components and metabolites via the liver portal vein ( 26 ). Increasing studies show that the gut–liver axis influences the progression of liver diseases such as liver inflammation, fibrosis, cirrhosis, and cancer ( 27 , 28 ). For instance, high-alcohol-producing bacterium Klebsiella pneumoniae is implicated in the pathogenesis of NAFLD in human patients, evidenced by oral gavage of a clinically isolated strain causing NAFLD in mice ( 29 ).…”

Section: The Roles Of Gut Microbiota In Liver Cancermentioning

confidence: 99%

The Potential Gut Microbiota-Mediated Treatment Options for Liver Cancer

2020

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Primary liver cancer is one of the leading causes of cancer death worldwide. Surgical and non-surgical treatments are optional for liver cancer therapy based on the cancer stage. Accumulating studies show that the gut–liver axis influences the progression of liver diseases, including liver inflammation, fibrosis, cirrhosis, and cancer. However, the role of gut microbiota and their derived components and metabolites in liver cancer remains to be further clarified. In this review, we discuss the roles of gut microbiota and specific bacterial species in HCC and the strategies to modulate gut microbiota to improve antitumor therapy. Given the limitation of current treatments, gut microbiota-mediated therapy is a potential option for HCC treatment, including fiber diet and vegetable diet, antimicrobials, probiotics, and pharmaceutical inhibitors. Also, gut microbiota can be used as a marker for early diagnosis of HCC. HCC occurs dependent on various environmental and genetic factors, including diet and sex. Furthermore, gut microbiota impacts the immunotherapy of HCC treatment. Therefore, a better understanding of the role of the gut–liver axis in liver cancer is critically important to improve therapeutic efficacy.

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“…Gut microbiota component and their metabolites affect both hepatocytes and stromal cells (hepatic stellate cells and Kupffer cells). [24] Intestinal dysbiosis is observed in different chronic hepatic diseases; which increased concern about its role in the development and progression of hepatic diseases with aggravation of liver disease-related complications. [25][26] Few studies evaluated the role of gut dysbiosis in patients with viral hepatitis.…”

Section: Variablesmentioning

confidence: 99%

Gut Microbiota Characterization in Patients with HCC Post Chronic HCV Infection

Montasser¹,

Osman²,

Abozaid³

et al. 2020

Preprint

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Aim: Dysbiosis of gut microbiota favors chronic hepatic inflammation with subsequent hepatic carcinogenesis. The current study aimed to evaluate the role of gut dysbiosis in the development of hepatocellular carcinoma in patients with chronic HCV infection.Methods: This descriptive cross-sectional cohort study carried out on 400 subjects recruited from the Internal Medicine Department and Tropical Medicine and Gastroenterology Department of Helwan and South Valley University Hospitals in Egypt. The study period was from January 2017 till January 2020. The subjects were divided clinically into three groups. Group I: One hundred patients with HCC, evaluated by Child Pugh, TNM and BCLC scoring systems. Group II: 200 chronic hepatitis C virus-infected patients. All patients infected with hepatitis C virus genotype 4. Group III: One hundred healthy control subjects with negative hepatitis marker and normal abdominal ultrasound. PCR of stool Microbiota, complete blood counts, complete liver function tests, INR, HCV antibodies and HBsAg were done for all included subjects. HCV PCR assessment and alpha-fetoprotein (AFP) were done for all patients.Results: No statistically significant difference was detected between HCC patients and control (p-value > 0.05) as regard Bacteroides fragilis & Akkermansia muciniphila. Faecalibacterium prausnitzii was less detected in HCC patients (51%), opposite to 70% of healthy control. With Statistically significant difference (p-value < 0.05). Bifidobacterium was less detected in HCC patients (43%), opposite to (76%) of healthy control. With highly statistically significant difference (p-value < 0.001). Lactobacillus & Enterobacteriaceae was more detected in HCC patients (80%) and (81%), in. Opposite to (36%) and (58%) in healthy control, respectively. With highly statistically significant difference (p-value < 0.001). no significant difference was detected between gut-microbiota and HCC progression with respect to Child or TNM systems. However, a significant difference was detected between number of positive stool isolate of Bacteroid Fragilis and BCLC staging system; where it was isolated from 66.7% of patients with BCLC stage IV opposite to 10.7% of patients with BCLC stage I.Conclusion: A characteristic pattern of Bifidobacterium, Lactobacillus and Enterobacteriaceae species in patients with chronic HCV and HCC was detected. Alteration of gut microbiota may be accused as a predisposing factor for liver disease progression.

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Role of the Gut–Liver Axis in Liver Inflammation, Fibrosis, and Cancer: A Special Focus on the Gut Microbiota Relationship

Cited by 138 publications

References 126 publications

Human FcRn expression and Type I Interferon signaling control Echovirus 11 pathogenesis in mice

Human FcRn expression and Type I Interferon signaling control Echovirus 11 pathogenesis in mice

The Potential Gut Microbiota-Mediated Treatment Options for Liver Cancer

Gut Microbiota Characterization in Patients with HCC Post Chronic HCV Infection

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